Gastric outlet obstruction: Difference between revisions
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{{SK}} GOO | {{SK}} GOO | ||
==Overview== | ==Overview== | ||
Gastric outlet obstruction occurs due to pathologies that cause intrinsic or extrinsic obstruction of the pylorus and antrum. Infiltration, scar formation or [[inflammation]] of the gastric outlet leads to intrinsic obstruction, while malignancy of neighboring structures such as the pancreas, gallbladder, liver and duodenum may lead to extrinsic [[obstruction]] of the gastric outlet. Common causes of GOO include [[Peptic ulcer|PUD]], gastric polyps, caustic ingestion, duodenal stricture, systemic [[amyloidosis]] of the [[gastrointestinal tract|gastrointestinal tract,]] eosinophillic [[gastroenteritis]] and obstruction by [[Gallstone disease|gallstones.]] Five percent of all cases of [[Peptic ulcer|peptic ulcer disease]] (which is the most common benign cause of GOO) worldwide, develop gastric outlet obstruction. GOO presents as nausea, vomiting, dehydration, electrolyte abnormalities, weight loss, malnutrition, fullness of [[epigastrium]], early satiety and bloating. Laboratory studies of patients may show [[Hypokalemia|hypokalemic]] [[Hypochloremia|hypochloremic]] [[metabolic alkalosis]] which is a characteristic feature due to [[Nausea and vomiting|vomiting]]. In case of of GOO due to suspected PUD, tests for H pylori should also be performed in patients. [[Upper gastrointestinal series|Barium upper GI studies]]<nowiki/> help in the determination of site of [[obstruction]], visualization of the [[Stomach|gastric]] silhouette, presence of gastric [[dilation]], pylorus narrowing, presence of ulcers, tumors and differentiation from gastroparesis. [[Esophagogastroduodenoscopy|Upper endoscopy]] performed in patients may help with visualization of the [[Stomach|gastric]] outlet, biopsy sampling in case of [[Lumen (anatomy)|intraluminal]] [[pathology]] and thereby helps rule out the presence of [[Cancer|malignancy]] in [[Patient|patients]] with symptoms of [[Peptic ulcer| | Gastric outlet obstruction (GOO) occurs due to pathologies that cause intrinsic or extrinsic obstruction of the pylorus and antrum. Infiltration, scar formation or [[inflammation]] of the gastric outlet leads to intrinsic obstruction, while malignancy of neighboring structures such as the pancreas, gallbladder, liver and duodenum may lead to extrinsic [[obstruction]] of the gastric outlet. Common causes of GOO include [[Peptic ulcer|peptic ulcer disease (PUD)]], gastric polyps, caustic ingestion, duodenal stricture, systemic [[amyloidosis]] of the [[gastrointestinal tract|gastrointestinal tract,]] eosinophillic [[gastroenteritis]] and obstruction by [[Gallstone disease|gallstones.]] Five percent of all cases of [[Peptic ulcer|peptic ulcer disease]] (which is the most common benign cause of GOO) worldwide, develop gastric outlet obstruction. GOO presents as nausea, vomiting, dehydration, electrolyte abnormalities, weight loss, malnutrition, fullness of [[epigastrium]], early satiety and bloating. Laboratory studies of patients may show [[Hypokalemia|hypokalemic]] [[Hypochloremia|hypochloremic]] [[metabolic alkalosis]] which is a characteristic feature due to [[Nausea and vomiting|vomiting]]. In case of of GOO due to suspected PUD, tests for H pylori should also be performed in patients. [[Upper gastrointestinal series|Barium upper GI studies]]<nowiki/> help in the determination of site of [[obstruction]], visualization of the [[Stomach|gastric]] silhouette, presence of gastric [[dilation]], pylorus narrowing, presence of ulcers, tumors and differentiation from gastroparesis. [[Esophagogastroduodenoscopy|Upper endoscopy]] performed in patients may help with visualization of the [[Stomach|gastric]] outlet, biopsy sampling in case of [[Lumen (anatomy)|intraluminal]] [[pathology]] and thereby helps rule out the presence of [[Cancer|malignancy]] in [[Patient|patients]] with symptoms of [[Peptic ulcer|peptic ulcer disease]]. Surgery is the primary modality of treatment for [[Patient|patients]] with GOO. It is required for more than 75 percent of patients with [[Scar|scarring]], [[fibrosis]], and [[Tumor|tumors]]. The aims of surgery in case of GOO include relief of [[obstruction]], relief in [[Patient|patients]] with failure to respond to medical therapy or failure to improve even after 72 hours of therapy and correction of [[Peptic ulcer|PUD]] symptoms. Various types of surgical procedures performed in cases of GOO are [[vagotomy]] and [[antrectomy]], [[gastrojejunostomy]] ([[vagotomy]] and [[antrectomy]] with Billroth II reconstruction), balloon [[Dilation|dilatation]], pylorotomy, pyloroplasty and laparoscopic techniques. Care must be taken to look out for various complications arising after [[surgery]] such as perforation, anastomotic leak, dilation and dysmotility of [[stomach]], edema of the [[Stomach|gastric]] wall and postgastrectomy syndromes. | ||
==Classification== | ==Classification== | ||
Gastric outlet obstruction (GOO) may be due to any underlying condition that results in mechanical [[obstruction]] to emptying of [[Stomach|gastric]] contents. GOO is classified based on the underlying cause into [[benign]] GOO and [[malignant]] GOO. Statistically, [[benign]] GOO comprises | Gastric outlet obstruction (GOO) may be due to any underlying condition that results in mechanical [[obstruction]] to emptying of [[Stomach|gastric]] contents. GOO is classified based on the underlying cause into [[benign]] GOO and [[malignant]] GOO. Statistically, [[benign]] GOO comprises 37 percent of cases and includes [[Peptic ulcer|peptic ulcer disease]] whereas malignant GOO comprises of the remaining 53 percent of cases. | ||
==Pathophysiology== | ==Pathophysiology== | ||
It is understood that GOO is the result of multiple intrinsic (lumen & wall) or extrinsic (involving neighbouring structures) pathologies that involve the [[antrum]] and the [[pylorus]]. | It is understood that GOO is the result of multiple intrinsic (lumen & wall) or extrinsic (involving neighbouring structures) pathologies that involve the [[antrum]] and the [[pylorus]]. | ||
* Intrinsic [[obstruction]]: Conditions involving infiltration, scar formation or [[inflammation]] of [[antrum]] and the [[pylorus]] may lead to intrinsic obstruction and GOO. | * Intrinsic [[obstruction]]: Conditions involving infiltration, scar formation or [[inflammation]] of [[antrum]] and the [[pylorus]] may lead to intrinsic obstruction and GOO. | ||
* Extrinsic [[obstruction]]: Any malignancy of neighboring structures such as duodenum, liver, gallbladder and pancreas may lead to extrinsic [[obstruction]] of gastric outlet. | * Extrinsic [[obstruction]]: Any [[malignancy]] of neighboring structures such as [[duodenum]], [[liver]], [[gallbladder]] and [[pancreas]] may lead to extrinsic [[obstruction]] of gastric outlet. | ||
==Causes== | ==Causes== | ||
Causes of GOO may be classified as benign and malignant. | Causes of GOO may be classified as [[benign]] and [[malignant]]. | ||
==== Benign causes ==== | ==== Benign causes ==== | ||
Benign causes of GOO can either be congenital or acquired. The [[Acquired disorder|acquired]] causes of GOO may further be categorized into acute or chronic. The acquired acute causes of GOO results from [[edema]] and [[inflammation]] of [[antrum]] and the [[pylorus]]. The acquired chronic causes of GOO results from intrinsic [[obstruction]] due to [[fibrosis]] and [[scar]] formation. In general, benign causes of GOO include: <ref name="pmid7235767">{{cite journal |vauthors=Bradley EL, Clements JL |title=Idiopathic duodenal obstruction: an unappreciated complication of pancreatitis |journal=Ann. Surg. |volume=193 |issue=5 |pages=638–48 |year=1981 |pmid=7235767 |pmc=1345138 |doi= |url=}}</ref><ref name="pmid1539568">{{cite journal |vauthors=Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK |title=Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history |journal=Am. J. Gastroenterol. |volume=87 |issue=3 |pages=337–41 |year=1992 |pmid=1539568 |doi= |url=}}</ref><ref name="pmid15332026">{{cite journal |vauthors=Poley JW, Steyerberg EW, Kuipers EJ, Dees J, Hartmans R, Tilanus HW, Siersema PD |title=Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy |journal=Gastrointest. Endosc. |volume=60 |issue=3 |pages=372–7 |year=2004 |pmid=15332026 |doi= |url=}}</ref><ref name="pmid10079337">{{cite journal |vauthors=Ciftci AO, Senocak ME, Büyükpamukçu N, Hiçsönmez A |title=Gastric outlet obstruction due to corrosive ingestion: incidence and outcome |journal=Pediatr. Surg. Int. |volume=15 |issue=2 |pages=88–91 |year=1999 |pmid=10079337 |doi=10.1007/s003830050523 |url=}}</ref> | Benign causes of GOO can either be congenital or acquired. The [[Acquired disorder|acquired]] causes of GOO may further be categorized into acute or chronic. The acquired acute causes of GOO results from [[edema]] and [[inflammation]] of [[antrum]] and the [[pylorus]]. The acquired chronic causes of GOO results from intrinsic [[obstruction]] due to [[fibrosis]] and [[scar]] formation. In general, benign causes of GOO include:<ref name="pmid7235767">{{cite journal |vauthors=Bradley EL, Clements JL |title=Idiopathic duodenal obstruction: an unappreciated complication of pancreatitis |journal=Ann. Surg. |volume=193 |issue=5 |pages=638–48 |year=1981 |pmid=7235767 |pmc=1345138 |doi= |url=}}</ref><ref name="pmid1539568">{{cite journal |vauthors=Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK |title=Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history |journal=Am. J. Gastroenterol. |volume=87 |issue=3 |pages=337–41 |year=1992 |pmid=1539568 |doi= |url=}}</ref><ref name="pmid15332026">{{cite journal |vauthors=Poley JW, Steyerberg EW, Kuipers EJ, Dees J, Hartmans R, Tilanus HW, Siersema PD |title=Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy |journal=Gastrointest. Endosc. |volume=60 |issue=3 |pages=372–7 |year=2004 |pmid=15332026 |doi= |url=}}</ref><ref name="pmid10079337">{{cite journal |vauthors=Ciftci AO, Senocak ME, Büyükpamukçu N, Hiçsönmez A |title=Gastric outlet obstruction due to corrosive ingestion: incidence and outcome |journal=Pediatr. Surg. Int. |volume=15 |issue=2 |pages=88–91 |year=1999 |pmid=10079337 |doi=10.1007/s003830050523 |url=}}</ref> | ||
* [[Peptic ulcer|PUD]]: 5% cases (most commonly affecting [[pylorus]] and initial part of the [[duodenum]]) | * [[GI]] causes such as [[Peptic ulcer|PUD]]: approximately 5% cases (most commonly affecting [[pylorus]] and initial part of the [[duodenum]]), [[Fundic gland polyposis|gastric polyps]], [[Stricture|duodenal stricture]], gastro-[[Duodenum|duodenal]] [[tuberculosis]], [[Caustic|caustic ingestion]], obstruction by [[Gallstone disease|gallstones]] (Bouveret syndrome), and [[pancreatic pseudocyst]] formation. | ||
[[Congenital]] causes of gastric outlet obstruction include:<ref name="pmid18668780">{{cite journal |vauthors=Kreel L, Ellis H |title=Pyloric stenosis in adults: A clinical and radiological study of 100 consecutive patients |journal=Gut |volume=6 |issue=3 |pages=253–61 |year=1965 |pmid=18668780 |pmc=1552275 |doi= |url=}}</ref><ref name="pmid12145672">{{cite journal |vauthors=Gheorghe L, Băncilă I, Gheorghe C, Herlea V, Vasilescu C, Aposteanu G |title=Antro-duodenal tuberculosis causing gastric outlet obstruction--a rare presentation of a protean disease |journal=Rom J Gastroenterol |volume=11 |issue=2 |pages=149–52 |year=2002 |pmid=12145672 |doi= |url=}}</ref> | |||
* [[Pyloric stenosis]]: It is due to [[Hypertrophy (medical)|hypertrophy]] of [[Pyloric antrum|pyloric]] [[Smooth muscle|smooth muscles]] (circular). [[Pyloric stenosis]] is the most common cause of GOO in children with boys more commonly affected than girls. | |||
* [[Pyloric stenosis]]:It is due to [[Hypertrophy (medical)|hypertrophy]] of [[Pyloric antrum|pyloric]] [[Smooth muscle|smooth muscles]] (circular). Pyloric stenosis is the most common cause of GOO in children with boys more commonly affected than girls. | |||
* [[Annular pancreas]]<ref name="pmid7771437">{{cite journal |vauthors=Urayama S, Kozarek R, Ball T, Brandabur J, Traverso L, Ryan J, Wechter D |title=Presentation and treatment of annular pancreas in an adult population |journal=Am. J. Gastroenterol. |volume=90 |issue=6 |pages=995–9 |year=1995 |pmid=7771437 |doi= |url=}}</ref> | * [[Annular pancreas]]<ref name="pmid7771437">{{cite journal |vauthors=Urayama S, Kozarek R, Ball T, Brandabur J, Traverso L, Ryan J, Wechter D |title=Presentation and treatment of annular pancreas in an adult population |journal=Am. J. Gastroenterol. |volume=90 |issue=6 |pages=995–9 |year=1995 |pmid=7771437 |doi= |url=}}</ref> | ||
==== Malignant causes ==== | ==== Malignant causes ==== | ||
* [[Cancer|Malignancies]] involving neighboring structures may lead to GOO:<ref name="pmid7572886">{{cite journal |vauthors=Johnson CD |title=Gastric outlet obstruction malignant until proved otherwise |journal=Am. J. Gastroenterol. |volume=90 |issue=10 |pages=1740 |year=1995 |pmid=7572886 |doi= |url=}}</ref><ref name="pmid7572891">{{cite journal |vauthors=Shone DN, Nikoomanesh P, Smith-Meek MM, Bender JS |title=Malignancy is the most common cause of gastric outlet obstruction in the era of H2 blockers |journal=Am. J. Gastroenterol. |volume=90 |issue=10 |pages=1769–70 |year=1995 |pmid=7572891 |doi= |url=}}</ref><ref name="pmid2207566">{{cite journal |vauthors=Johnson CD, Ellis H |title=Gastric outlet obstruction now predicts malignancy |journal=Br J Surg |volume=77 |issue=9 |pages=1023–4 |year=1990 |pmid=2207566 |doi= | * [[Cancer|Malignancies]] involving neighboring structures may lead to GOO:<ref name="pmid7572886">{{cite journal |vauthors=Johnson CD |title=Gastric outlet obstruction malignant until proved otherwise |journal=Am. J. Gastroenterol. |volume=90 |issue=10 |pages=1740 |year=1995 |pmid=7572886 |doi= |url=}}</ref><ref name="pmid7572891">{{cite journal |vauthors=Shone DN, Nikoomanesh P, Smith-Meek MM, Bender JS |title=Malignancy is the most common cause of gastric outlet obstruction in the era of H2 blockers |journal=Am. J. Gastroenterol. |volume=90 |issue=10 |pages=1769–70 |year=1995 |pmid=7572891 |doi= |url=}}</ref><ref name="pmid2207566">{{cite journal |vauthors=Johnson CD, Ellis H |title=Gastric outlet obstruction now predicts malignancy |journal=Br J Surg |volume=77 |issue=9 |pages=1023–4 |year=1990 |pmid=2207566 |doi= |url=}}</ref> | ||
** [[Pancreas]]: [[Pancreatic cancer]] | ** [[Pancreas]]: [[Pancreatic cancer]] | ||
*** Most common [[Cancer|malignancy]] leading to extrinsic [[obstruction]] of the [[pylorus]] | *** Most common [[Cancer|malignancy]] leading to extrinsic [[obstruction]] of the [[pylorus]] | ||
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==Differentiating {{PAGENAME}} from Other Diseases== | ==Differentiating {{PAGENAME}} from Other Diseases== | ||
Gastric outlet obstruction must be differentiated from other conditions that cause abdominal pain, heartburn, bloating, nausea and vomiting such as:<ref name="pmid6710074">{{cite journal| author=Sugimachi K, Inokuchi K, Kuwano H, Ooiwa T| title=Acute gastritis clinically classified in accordance with data from both upper GI series and endoscopy. | journal=Scand J Gastroenterol | year= 1984 | volume= 19 | issue= 1 | pages= 31-7 | pmid=6710074 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6710074 }} </ref><ref name="pmid25901896">{{cite journal| author=Sipponen P, Maaroos HI| title=Chronic gastritis. | journal=Scand J Gastroenterol | year= 2015 | volume= 50 | issue= 6 | pages= 657-67 | pmid=25901896 | doi=10.3109/00365521.2015.1019918 | pmc=4673514 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25901896 }} </ref><ref name="pmid16819502">{{cite journal| author=Sartor RB| title=Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis. | journal=Nat Clin Pract Gastroenterol Hepatol | year= 2006 | volume= 3 | issue= 7 | pages= 390-407 | pmid=16819502 | doi=10.1038/ncpgasthep0528 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16819502 }} </ref><ref name="pmid2789799">{{cite journal| author=Sipponen P| title=Atrophic gastritis as a premalignant condition. | journal=Ann Med | year= 1989 | volume= 21 | issue= 4 | pages= 287-90 | pmid=2789799 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2789799 }} </ref><ref name="pmid25133039">{{cite journal| author=Badillo R, Francis D| title=Diagnosis and treatment of gastroesophageal reflux disease. | journal=World J Gastrointest Pharmacol Ther | year= 2014 | volume= 5 | issue= 3 | pages= 105-12 | pmid=25133039 | doi=10.4292/wjgpt.v5.i3.105 | pmc=4133436 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25133039 }} </ref><ref name="pmid17956071">{{cite journal| author=Ramakrishnan K, Salinas RC| title=Peptic ulcer disease. | journal=Am Fam Physician | year= 2007 | volume= 76 | issue= 7 | pages= 1005-12 | pmid=17956071 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17956071 }} </ref><ref name="pmid17985090">{{cite journal| author=Banasch M, Schmitz F| title=Diagnosis and treatment of gastrinoma in the era of proton pump inhibitors. | journal=Wien Klin Wochenschr | year= 2007 | volume= 119 | issue= 19-20 | pages= 573-8 | pmid=17985090 | doi=10.1007/s00508-007-0884-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17985090 }} </ref><ref name="pmid15621988">{{cite journal| author=Dicken BJ, Bigam DL, Cass C, Mackey JR, Joy AA, Hamilton SM| title=Gastric adenocarcinoma: review and considerations for future directions. | journal=Ann Surg | year= 2005 | volume= 241 | issue= 1 | pages= 27-39 | pmid=15621988 | doi= | pmc=1356843 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15621988 }} </ref><ref name="pmid21390139">{{cite journal| author=Ghimire P, Wu GY, Zhu L| title=Primary gastrointestinal lymphoma. | journal=World J Gastroenterol | year= 2011 | volume= 17 | issue= 6 | pages= 697-707 | pmid=21390139 | doi=10.3748/wjg.v17.i6.697 | pmc=3042647 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21390139 }} </ref> | |||
{| class="wikitable" style="border: 0px; font-size: 90%; margin: 3px;" align="center" | {| class="wikitable" style="border: 0px; font-size: 90%; margin: 3px;" align="center" | ||
| colspan="12" style="background: #4479BA; text-align: center;" | {{fontcolor|#FFF|'''Differential Diagnosis'''}} | | colspan="12" style="background: #4479BA; text-align: center;" | {{fontcolor|#FFF|'''Differential Diagnosis'''}} | ||
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|✔ | |✔ | ||
|✔ | |✔ | ||
|[[Melena|Black stools]] in case of [[Peptic ulcer| | |[[Melena|Black stools]] in case of [[Peptic ulcer|peptic ulcer disease(PUD)]] | ||
| | | | ||
* Determines the site of [[obstruction]] | * Determines the site of [[obstruction]] | ||
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|✔ | |✔ | ||
( | (Suspect [[gastric outlet obstruction]]) | ||
|✔ | |✔ | ||
|<nowiki>-</nowiki> | |<nowiki>-</nowiki> | ||
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* Night sweats | * Night sweats | ||
|} | |} | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
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==Diagnosis== | ==Diagnosis== | ||
===History | ===History === | ||
The following history is relevant in patients with GOO:<ref name="pmid3602991">{{cite journal |vauthors=Green ST, Drury JK, McCallion J, Erwin L |title=Carcinoid tumour presenting as recurrent gastric outlet obstruction: a case of long-term survival |journal=Scott Med J |volume=32 |issue=2 |pages=54–5 |year=1987 |pmid=3602991 |doi=10.1177/003693308703200212 |url=}}</ref><ref name="pmid8759707">{{cite journal |vauthors=Chowdhury A, Dhali GK, Banerjee PK |title=Etiology of gastric outlet obstruction |journal=Am. J. Gastroenterol. |volume=91 |issue=8 |pages=1679 |year=1996 |pmid=8759707 |doi= |url=}}</ref> | The following history is relevant in patients with GOO:<ref name="pmid3602991">{{cite journal |vauthors=Green ST, Drury JK, McCallion J, Erwin L |title=Carcinoid tumour presenting as recurrent gastric outlet obstruction: a case of long-term survival |journal=Scott Med J |volume=32 |issue=2 |pages=54–5 |year=1987 |pmid=3602991 |doi=10.1177/003693308703200212 |url=}}</ref><ref name="pmid8759707">{{cite journal |vauthors=Chowdhury A, Dhali GK, Banerjee PK |title=Etiology of gastric outlet obstruction |journal=Am. J. Gastroenterol. |volume=91 |issue=8 |pages=1679 |year=1996 |pmid=8759707 |doi= |url=}}</ref> | ||
* History of [[Peptic ulcer| | * History of [[Peptic ulcer|peptic ulcer disease]] or its complications | ||
* History of [[abdominal pain]] and [[weight loss]] in cases of [[pancreatic cancer]] | * History of [[abdominal pain]] and [[weight loss]] in cases of [[pancreatic cancer]] | ||
==== Symptoms ==== | |||
The clinical presentation of GOO is categorized into early and late stage symptoms. The early stage symptoms include nausea and vomiting (characteristic feature). [[Nausea and vomiting|Vomiting]] is intermittent, non [[Bile|bilious]], occurs after one hour after consuming meal and contains undigested particles of food leading to [[dehydration]].<ref name="pmid7129059">{{cite journal |vauthors=Miner PB, Harri JE, McPhee MS |title=Intermittent gastric outlet obstruction from a pedunculated gastric polyp |journal=Gastrointest. Endosc. |volume=28 |issue=3 |pages=219–20 |year=1982 |pmid=7129059 |doi= |url=}}</ref><ref name="pmid7771437">{{cite journal |vauthors=Urayama S, Kozarek R, Ball T, Brandabur J, Traverso L, Ryan J, Wechter D |title=Presentation and treatment of annular pancreas in an adult population |journal=Am. J. Gastroenterol. |volume=90 |issue=6 |pages=995–9 |year=1995 |pmid=7771437 |doi= |url=}}</ref> | |||
The late stage symptoms include abdominal fullness, [[malnutrition]], [[weight loss]], [[bloating]], and early satiety.<ref name="pmid7572891">{{cite journal |vauthors=Shone DN, Nikoomanesh P, Smith-Meek MM, Bender JS |title=Malignancy is the most common cause of gastric outlet obstruction in the era of H2 blockers |journal=Am. J. Gastroenterol. |volume=90 |issue=10 |pages=1769–70 |year=1995 |pmid=7572891 |doi= |url=}}</ref><ref name="pmid16817848">{{cite journal |vauthors=Cappell MS, Davis M |title=Characterization of Bouveret's syndrome: a comprehensive review of 128 cases |journal=Am. J. Gastroenterol. |volume=101 |issue=9 |pages=2139–46 |year=2006 |pmid=16817848 |doi=10.1111/j.1572-0241.2006.00645.x |url=}}</ref> | |||
===Physical Examination=== | ===Physical Examination=== | ||
In the late stages of GOO, patients may develop signs of [[malnutrition]] and incomplete [[obstruction]]. Signs of malnutrition include weight loss and signs of [[dehydration]]. Signs of incomplete obstruction include findings such as [[abdominal mass]], visible [[Stomach|gastric]] [[peristalsis]], fullness of [[epigastrium]] and a tympanitic mass on percussion. | In the late stages of GOO, patients may develop signs of [[malnutrition]] and incomplete [[obstruction]]. Signs of malnutrition include weight loss and signs of [[dehydration]]. Signs of incomplete [[obstruction]] include findings such as [[abdominal mass]], visible [[Stomach|gastric]] [[peristalsis]], fullness of [[epigastrium]] and a tympanitic mass on percussion. | ||
{{#ev:youtube|UVJYQlUm2A8}} | {{#ev:youtube|UVJYQlUm2A8}} | ||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
Laboratory investigations suggestive of GOO include [[Hypokalemia| | Laboratory investigations suggestive of GOO include [[Hypokalemia|hypokalemic]] [[Hypochloremia|hypochloremic]] [[metabolic alkalosis]] (due to vomiting). In order to assess the severity and etiology of GOO, other investigations such as CBC, electrolyte panel, tests for H Pylori and [[liver function tests]] may be done.<ref name="pmid2760432">{{cite journal |vauthors=Hangen D, Maltz GS, Anderson JE, Knauer CM |title=Marked hypergastrinemia in gastric outlet obstruction |journal=J. Clin. Gastroenterol. |volume=11 |issue=4 |pages=442–4 |year=1989 |pmid=2760432 |doi= |url=}}</ref> | ||
===Imaging Findings=== | ===Imaging Findings=== | ||
Imaging studies such as [[Radiography|plain radiographs]], [[Radiocontrast|contrast]] [[Upper gastrointestinal series|upper gastrointestinal (GI) studies]] and [[Computed Tomography| | Imaging studies such as [[Radiography|plain radiographs]], [[Radiocontrast|contrast]] [[Upper gastrointestinal series|upper gastrointestinal (GI) studies]] and [[Computed Tomography|computed tomography (CT)]] with [[Radiocontrast|oral contrast]] may be used for evaluating patients with [[Symptom|symptoms]] of GOO. | ||
'''X ray''' | '''X ray''' | ||
An | An X-ray (obstruction series or barium study) may be helpful in the diagnosis of GOO. Findings on an x-ray suggestive of GOO include [[Stomach|gastric]] [[Dilation|dilatation]]. Findings on barium or Gastrografin study help in the determination of site of [[obstruction]], visualization of the [[Stomach|gastric]] silhouette, [[Stomach|gastric]] [[dilation]], narrowed [[pylorus]], presence of [[Ulcer|ulcers]] and tumors. GOO may also be differentiated from [[gastroparesis]] in which gastric [[dilation]] is not associated with the narrowing of the [[pylorus]]. | ||
* [[Nuclear medicine|Nuclear gastric emptying study]]:<ref name="pmid1199997">{{cite journal |vauthors=Chaudhuri TK, Greenwald AJ, Heading RC |title=Measurement of gastric emptying time--a comparative study between nonisotopic aspiration method and new radioisotopic technique |journal=Am J Dig Dis |volume=20 |issue=11 |pages=1063–6 |year=1975 |pmid=1199997 |doi= |url=}}</ref> | * [[Nuclear medicine|Nuclear gastric emptying study]]:<ref name="pmid1199997">{{cite journal |vauthors=Chaudhuri TK, Greenwald AJ, Heading RC |title=Measurement of gastric emptying time--a comparative study between nonisotopic aspiration method and new radioisotopic technique |journal=Am J Dig Dis |volume=20 |issue=11 |pages=1063–6 |year=1975 |pmid=1199997 |doi= |url=}}</ref> | ||
** [[Radionuclide]] is given orally and its passage is measured over a certain duration. | ** [[Radionuclide]] is given orally and its passage is measured over a certain duration. | ||
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==== Endoscopy ==== | ==== Endoscopy ==== | ||
[[Esophagogastroduodenoscopy|Upper endoscopy]] may be helpful in the diagnosis of GOO. An upper endoscopy aids in visualization of the [[Stomach|gastric]] outlet, [[ | [[Esophagogastroduodenoscopy|Upper endoscopy]] may be helpful in the diagnosis of GOO. An upper endoscopy aids in visualization of the [[Stomach|gastric]] outlet, [[biopsy]] sampling in case of [[Lumen (anatomy)|intraluminal]] [[pathology]]. In addition, endoscopic [[biopsy]] helps rule out the presence of [[Cancer|malignancy]] in [[Patient|patients]] with symptoms of [[Peptic ulcer|peptic ulcer disease (PUD)]]:<ref name="pmid8635729">{{cite journal |vauthors=Lau JY, Chung SC, Sung JJ, Chan AC, Ng EK, Suen RC, Li AK |title=Through-the-scope balloon dilation for pyloric stenosis: long-term results |journal=Gastrointest. Endosc. |volume=43 |issue=2 Pt 1 |pages=98–101 |year=1996 |pmid=8635729 |doi= |url=}}</ref><ref name="pmid9831838">{{cite journal |vauthors=Awan A, Johnston DE, Jamal MM |title=Gastric outlet obstruction with benign endoscopic biopsy should be further explored for malignancy |journal=Gastrointest. Endosc. |volume=48 |issue=5 |pages=497–500 |year=1998 |pmid=9831838 |doi= |url=}}</ref> | ||
==== Sodium chloride load test ==== | ==== Sodium chloride load test ==== | ||
In sodium chloride test, the patient is infused with 750 | In sodium chloride test, the patient is infused with 750 mililiters of [[sodium chloride]] solution into the [[stomach]] via a [[Nasogastric tube|nasogastric tube (NGT)]]. After half an hour if > 400 mL is left in the [[stomach]], the diagnosis of GOO is made.<ref name="pmid5831782">{{cite journal |vauthors=Goldstein H, Boyle JD |title=The saline load test--a bedside evaluation of gastric retention |journal=Gastroenterology |volume=49 |issue=4 |pages=375–80 |year=1965 |pmid=5831782 |doi= |url=}}</ref> | ||
==== Needle-guided biopsy ==== | ==== Needle-guided biopsy ==== | ||
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==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
* Medical therapy may be given to all [[Patient|patients]] prior to [[surgery]] in cases of | * Medical therapy may be given to all [[Patient|patients]] prior to [[surgery]] in cases of gastric outlet obstruction. Medical therapy primarily involves supportive care in preparation of surgery with hydration, NG tube decompression, correction of [[Electrolyte disturbance|electrolyte imbalances]]. <ref name="pmid10436838">{{cite journal |vauthors=Gouma DJ, van Geenen R, van Gulik T, de Wit LT, Obertop H |title=Surgical palliative treatment in bilio-pancreatic malignancy |journal=Ann. Oncol. |volume=10 Suppl 4 |issue= |pages=269–72 |year=1999 |pmid=10436838 |doi= |url=}}</ref> | ||
* [[Endoscopy|Endoscopic]] [[stent]] placement for advanced GI cancer causing GOO.<ref name="pmid15605026">{{cite journal |vauthors=Holt AP, Patel M, Ahmed MM |title=Palliation of patients with malignant gastroduodenal obstruction with self-expanding metallic stents: the treatment of choice? |journal=Gastrointest. Endosc. |volume=60 |issue=6 |pages=1010–7 |year=2004 |pmid=15605026 |doi= |url=}}</ref> | |||
* | |||
* In patients with benign Gastric Outlet Obstruction due to [[Peptic ulcer| | * In patients with benign Gastric Outlet Obstruction due to [[Peptic ulcer|peptic ulcer disease]], medical therapy with proton pump inhibitors or histamine-2 (H2) blockers is given in [[Patient|patients]] to treat acute [[inflammation]] and [[edema]].<ref name="pmid7572891" /> | ||
* For the treatment of [[Stenosis|strictures]] in patients with GOO due to advanced stage [[cancer]], [[Endoscopy|endoscopic]] [[Pneumatic tube|pneumatic]] balloon [[Dilation|dilatation]] and use of [[Stent|self-expandable metallic stents]] are preferred techniques.<ref name="pmid8409292">{{cite journal |vauthors=Kozarek RA |title=Dilation therapy for gastric outlet obstruction. Are balloons a bust? |journal=J. Clin. Gastroenterol. |volume=17 |issue=1 |pages=2–4 |year=1993 |pmid=8409292 |doi= |url=}}</ref> | * For the treatment of [[Stenosis|strictures]] in patients with GOO due to advanced stage [[cancer]], [[Endoscopy|endoscopic]] [[Pneumatic tube|pneumatic]] balloon [[Dilation|dilatation]] and use of [[Stent|self-expandable metallic stents]] are preferred techniques.<ref name="pmid8409292">{{cite journal |vauthors=Kozarek RA |title=Dilation therapy for gastric outlet obstruction. Are balloons a bust? |journal=J. Clin. Gastroenterol. |volume=17 |issue=1 |pages=2–4 |year=1993 |pmid=8409292 |doi= |url=}}</ref> | ||
===Surgery=== | ===Surgery=== | ||
Surgery is the primary modality of treatment for [[Patient|patients]] with GOO. It is required for more than 75 percent of patients, with [[Scar|scarring]], [[fibrosis]] and [[Tumor|tumors]]. The aims of surgery in case of GOO include | Surgery is the primary modality of treatment for [[Patient|patients]] with GOO. It is required for more than 75 percent of patients, with [[Scar|scarring]], [[fibrosis]] and [[Tumor|tumors]]. The aims of surgery in case of GOO include relief of [[obstruction]], [[Patient|patients]] with failure to respond to medical therapy or failure to improve even after 72 hours of therapy, and correction of [[Peptic ulcer|PUD]] symptoms. | ||
==== Guidelines for surgery ==== | ==== Guidelines for surgery ==== | ||
Surgery should be considered only in patients who are able to tolerate the surgical procedure. Major [[Resection|resections]] of the [[tumor]] must be done in the absence of [[Metastasis|metastatic disease]]. In the case of [[Metastasis|metastatic disease]], extent of [[surgery]] needs to be determined. | |||
==== Types of surgical procedures ==== | ==== Types of surgical procedures ==== | ||
The types of surgical procedures performed in cases of GOO are as follows: | The types of surgical procedures performed in cases of GOO are as follows:<ref name="pmid12384765">{{cite journal |vauthors=Alam TA, Baines M, Parker MC |title=The management of gastric outlet obstruction secondary to inoperable cancer |journal=Surg Endosc |volume=17 |issue=2 |pages=320–3 |year=2003 |pmid=12384765 |doi=10.1007/s00464-001-9197-0 |url=}}</ref><ref name="pmid17640581">{{cite journal |vauthors=Chopita N, Landoni N, Ross A, Villaverde A |title=Malignant gastroenteric obstruction: therapeutic options |journal=Gastrointest. Endosc. Clin. N. Am. |volume=17 |issue=3 |pages=533–44, vi–vii |year=2007 |pmid=17640581 |doi=10.1016/j.giec.2007.05.007 |url=}}</ref><ref name="pmid11967685">{{cite journal |vauthors=Wong YT, Brams DM, Munson L, Sanders L, Heiss F, Chase M, Birkett DH |title=Gastric outlet obstruction secondary to pancreatic cancer: surgical vs endoscopic palliation |journal=Surg Endosc |volume=16 |issue=2 |pages=310–2 |year=2002 |pmid=11967685 |doi=10.1007/s00464-001-9061-2 |url=}}</ref> | ||
* Vagotomy and [[antrectomy]], gastrojejunostomy ([[vagotomy]] and [[antrectomy]] with Billroth II reconstruction), balloon [[Dilation|dilatation]], pylorotomy, [[pyloroplasty]], robotic-assisted [[pyloroplasty]], [[vagotomy]] and [[pyloroplasty]], truncal [[vagotomy]] and [[gastrojejunostomy]] and [[Laparoscopic surgery|laparoscopic]] surgery ([[Laparoscopic|laparoscopic truncal vagotomy]], [[Laparoscopic surgery|laparoscopic gastrojejunostomy]], [[Laparoscopic surgery|laparoscopic pyloromyotomy]], [[Laparoscopic surgery|laparoscopic gastrojejunostomy]]). The advantages of [[Laparoscopic surgery|laparoscopy]] include fast [[Gastrointestinal tract|GI]] transit recovery time, fewer [[Blood transfusion|blood transfusions]], low [[Mortality rate|mortality]] and brief hospital stay. | |||
* [[Endoscopy|Endoscopic surgery (Endoscopic gastroenteric anastomosis)]] is preferred in cases of [[malignant]] [[obstruction]]. The advantages include high success rate, brief hospital stay and low [[Mortality rate|mortality]].<ref name="pmid16046997">{{cite journal |vauthors=Kantsevoy SV, Jagannath SB, Niiyama H, Chung SS, Cotton PB, Gostout CJ, Hawes RH, Pasricha PJ, Magee CA, Vaughn CA, Barlow D, Shimonaka H, Kalloo AN |title=Endoscopic gastrojejunostomy with survival in a porcine model |journal=Gastrointest. Endosc. |volume=62 |issue=2 |pages=287–92 |year=2005 |pmid=16046997 |doi= |url=}}</ref><ref name="pmid15824939">{{cite journal |vauthors=Chopita N, Vaillaverde A, Cope C, Bernedo A, Martinez H, Landoni N, Jmelnitzky A, Burgos H |title=Endoscopic gastroenteric anastomosis using magnets |journal=Endoscopy |volume=37 |issue=4 |pages=313–7 |year=2005 |pmid=15824939 |doi=10.1055/s-2005-861358 |url=}}</ref><ref name="pmid23522025">{{cite journal |vauthors=No JH, Kim SW, Lim CH, Kim JS, Cho YK, Park JM, Lee IS, Choi MG, Choi KY |title=Long-term outcome of palliative therapy for gastric outlet obstruction caused by unresectable gastric cancer in patients with good performance status: endoscopic stenting versus surgery |journal=Gastrointest. Endosc. |volume=78 |issue=1 |pages=55–62 |year=2013 |pmid=23522025 |doi=10.1016/j.gie.2013.01.041 |url=}}</ref> | |||
==== Contraindications to surgery ==== | ==== Contraindications to surgery ==== | ||
Contraindications to [[surgery]] include | Contraindications to [[surgery]] include severe [[malnutrition]] and advanced unresectable [[cancer]]. | ||
==== Complications of surgery ==== | ==== Complications of surgery ==== | ||
Complications arising after [[surgery]] include | Complications arising after [[surgery]] include perforation due to [[Stent|stenting]], stent reocclusion, stent migration, stomach dilation, gastric wall edema, anastomotic leak and postgastrectomy syndromes.<ref name="pmid3970597">{{cite journal |vauthors=Jaffin BW, Kaye MD |title=The prognosis of gastric outlet obstruction |journal=Ann. Surg. |volume=201 |issue=2 |pages=176–9 |year=1985 |pmid=3970597 |pmc=1250637 |doi= |url=}}</ref><ref name="pmid8803569">{{cite journal |vauthors=Khullar SK, DiSario JA |title=Gastric outlet obstruction |journal=Gastrointest. Endosc. Clin. N. Am. |volume=6 |issue=3 |pages=585–603 |year=1996 |pmid=8803569 |doi= |url=}}</ref> | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} |
Latest revision as of 16:31, 15 February 2018
Gastric outlet obstruction Microchapters |
Differentiating Gastric outlet obstruction from other Diseases |
---|
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]
Synonyms and keywords: GOO
Overview
Gastric outlet obstruction (GOO) occurs due to pathologies that cause intrinsic or extrinsic obstruction of the pylorus and antrum. Infiltration, scar formation or inflammation of the gastric outlet leads to intrinsic obstruction, while malignancy of neighboring structures such as the pancreas, gallbladder, liver and duodenum may lead to extrinsic obstruction of the gastric outlet. Common causes of GOO include peptic ulcer disease (PUD), gastric polyps, caustic ingestion, duodenal stricture, systemic amyloidosis of the gastrointestinal tract, eosinophillic gastroenteritis and obstruction by gallstones. Five percent of all cases of peptic ulcer disease (which is the most common benign cause of GOO) worldwide, develop gastric outlet obstruction. GOO presents as nausea, vomiting, dehydration, electrolyte abnormalities, weight loss, malnutrition, fullness of epigastrium, early satiety and bloating. Laboratory studies of patients may show hypokalemic hypochloremic metabolic alkalosis which is a characteristic feature due to vomiting. In case of of GOO due to suspected PUD, tests for H pylori should also be performed in patients. Barium upper GI studies help in the determination of site of obstruction, visualization of the gastric silhouette, presence of gastric dilation, pylorus narrowing, presence of ulcers, tumors and differentiation from gastroparesis. Upper endoscopy performed in patients may help with visualization of the gastric outlet, biopsy sampling in case of intraluminal pathology and thereby helps rule out the presence of malignancy in patients with symptoms of peptic ulcer disease. Surgery is the primary modality of treatment for patients with GOO. It is required for more than 75 percent of patients with scarring, fibrosis, and tumors. The aims of surgery in case of GOO include relief of obstruction, relief in patients with failure to respond to medical therapy or failure to improve even after 72 hours of therapy and correction of PUD symptoms. Various types of surgical procedures performed in cases of GOO are vagotomy and antrectomy, gastrojejunostomy (vagotomy and antrectomy with Billroth II reconstruction), balloon dilatation, pylorotomy, pyloroplasty and laparoscopic techniques. Care must be taken to look out for various complications arising after surgery such as perforation, anastomotic leak, dilation and dysmotility of stomach, edema of the gastric wall and postgastrectomy syndromes.
Classification
Gastric outlet obstruction (GOO) may be due to any underlying condition that results in mechanical obstruction to emptying of gastric contents. GOO is classified based on the underlying cause into benign GOO and malignant GOO. Statistically, benign GOO comprises 37 percent of cases and includes peptic ulcer disease whereas malignant GOO comprises of the remaining 53 percent of cases.
Pathophysiology
It is understood that GOO is the result of multiple intrinsic (lumen & wall) or extrinsic (involving neighbouring structures) pathologies that involve the antrum and the pylorus.
- Intrinsic obstruction: Conditions involving infiltration, scar formation or inflammation of antrum and the pylorus may lead to intrinsic obstruction and GOO.
- Extrinsic obstruction: Any malignancy of neighboring structures such as duodenum, liver, gallbladder and pancreas may lead to extrinsic obstruction of gastric outlet.
Causes
Causes of GOO may be classified as benign and malignant.
Benign causes
Benign causes of GOO can either be congenital or acquired. The acquired causes of GOO may further be categorized into acute or chronic. The acquired acute causes of GOO results from edema and inflammation of antrum and the pylorus. The acquired chronic causes of GOO results from intrinsic obstruction due to fibrosis and scar formation. In general, benign causes of GOO include:[1][2][3][4]
- GI causes such as PUD: approximately 5% cases (most commonly affecting pylorus and initial part of the duodenum), gastric polyps, duodenal stricture, gastro-duodenal tuberculosis, caustic ingestion, obstruction by gallstones (Bouveret syndrome), and pancreatic pseudocyst formation.
Congenital causes of gastric outlet obstruction include:[5][6]
- Pyloric stenosis: It is due to hypertrophy of pyloric smooth muscles (circular). Pyloric stenosis is the most common cause of GOO in children with boys more commonly affected than girls.
- Annular pancreas[7]
Malignant causes
- Malignancies involving neighboring structures may lead to GOO:[8][9][10]
- Pancreas: Pancreatic cancer
- Most common malignancy leading to extrinsic obstruction of the pylorus
- Occurence in one fifth of patients
- Stomach: Gastric cancer, Zollinger-Ellison Syndrome [11]
- Duodenum: Duodenal cancer, ampullary cancer
- Bile duct: Cholangiocarcinoma
- Secondary metastasis to the gastric outlet by other primaries
- Pancreas: Pancreatic cancer
Differentiating Gastric outlet obstruction from Other Diseases
Gastric outlet obstruction must be differentiated from other conditions that cause abdominal pain, heartburn, bloating, nausea and vomiting such as:[12][13][14][15][16][17][18][19][20]
Differential Diagnosis | |||||||||||
Disease | Symptoms | Diagnosis | Other findings | ||||||||
Pain | Nausea & Vomiting | Heartburn | Belching or Bloating | Weight loss | Loss of Appetite | Stools | Endoscopy findings | ||||
Location | Aggravating Factors | Alleviating Factors | |||||||||
Gastric outlet obstruction (GOO) | Food | - | ✔ | ✔ | ✔ | ✔ | ✔ | Black stools in case of peptic ulcer disease(PUD) |
|
Sodium chloride load test
Needle-guided biopsy
| |
Acute gastritis | Food | Antacids | ✔ | ✔ | ✔ | - | ✔ | Black stools |
|
- | |
Chronic gastritis | Food | Antacids | ✔ | ✔ | ✔ | ✔ | ✔ | - | H. pylori gastritis
Lymphocytic gastritis
|
- | |
Atrophic gastritis | - | - | ✔ | - | ✔ | ✔ | - | H. pylori
|
Diagnosed by:
| ||
Crohn's disease | - | - | - | - | - | ✔ | ✔ |
|
|
||
GERD |
|
|
✔
(Suspect delayed gastric emptying) |
✔ | - | - | - | - | Other symptoms: | ||
Peptic ulcer disease |
|
|
|
✔ | ✔ | - | - | - | Gastric ulcers
Duodenal ulcers
|
Other diagnostic tests | |
Gastrinoma | - | - | ✔
(Suspect gastric outlet obstruction) |
✔ | - | - | - | Useful in collecting the tissue for biopsy |
Diagnostic tests
| ||
Gastric Adenocarcinoma | - | - | ✔ | ✔ | ✔ | ✔ | ✔ |
|
Esophagogastroduodenoscopy
|
Other symptoms | |
Primary gastric lymphoma | - | - | - | - | - | ✔ | - | - | Useful in collecting the tissue for biopsy | Other symptoms
|
Epidemiology and Demographics
The epidemiology of GOO is as follows:[21][22]
- The incidence of peptic ulcer disease (which is the most common benign cause of GOO) is approximately 10-19 per 100,000 individuals worldwide.
- Five percent of all cases of peptic ulcer disease worldwide, develop gastric outlet obstruction.
- The incidence of gastric outlet obstruction is less than 5 per 100,000 patients worldwide.
- In the United States, peptic ulcer disease requires an average of 2000 surgeries annually.
- Pancreatic cancer is the most common malignant cause of GOO.
- The incidence of GOO in cases with pancreatic cancer is approximately 20% of all cases.
Diagnosis
History
The following history is relevant in patients with GOO:[23][24]
- History of peptic ulcer disease or its complications
- History of abdominal pain and weight loss in cases of pancreatic cancer
Symptoms
The clinical presentation of GOO is categorized into early and late stage symptoms. The early stage symptoms include nausea and vomiting (characteristic feature). Vomiting is intermittent, non bilious, occurs after one hour after consuming meal and contains undigested particles of food leading to dehydration.[25][7]
The late stage symptoms include abdominal fullness, malnutrition, weight loss, bloating, and early satiety.[9][26]
Physical Examination
In the late stages of GOO, patients may develop signs of malnutrition and incomplete obstruction. Signs of malnutrition include weight loss and signs of dehydration. Signs of incomplete obstruction include findings such as abdominal mass, visible gastric peristalsis, fullness of epigastrium and a tympanitic mass on percussion. {{#ev:youtube|UVJYQlUm2A8}}
Laboratory Findings
Laboratory investigations suggestive of GOO include hypokalemic hypochloremic metabolic alkalosis (due to vomiting). In order to assess the severity and etiology of GOO, other investigations such as CBC, electrolyte panel, tests for H Pylori and liver function tests may be done.[27]
Imaging Findings
Imaging studies such as plain radiographs, contrast upper gastrointestinal (GI) studies and computed tomography (CT) with oral contrast may be used for evaluating patients with symptoms of GOO.
X ray
An X-ray (obstruction series or barium study) may be helpful in the diagnosis of GOO. Findings on an x-ray suggestive of GOO include gastric dilatation. Findings on barium or Gastrografin study help in the determination of site of obstruction, visualization of the gastric silhouette, gastric dilation, narrowed pylorus, presence of ulcers and tumors. GOO may also be differentiated from gastroparesis in which gastric dilation is not associated with the narrowing of the pylorus.
- Nuclear gastric emptying study:[28]
- Radionuclide is given orally and its passage is measured over a certain duration.
Computed tomography (CT) with oral contrast
CT with oral contrast or CT-guided biopsy may be done in suspected cases with equivocal findings on X Ray and Barium Upper GI studies. Findings of CT are variable and include those of the underlying condition.
Other Diagnostic Studies
Endoscopy
Upper endoscopy may be helpful in the diagnosis of GOO. An upper endoscopy aids in visualization of the gastric outlet, biopsy sampling in case of intraluminal pathology. In addition, endoscopic biopsy helps rule out the presence of malignancy in patients with symptoms of peptic ulcer disease (PUD):[29][30]
Sodium chloride load test
In sodium chloride test, the patient is infused with 750 mililiters of sodium chloride solution into the stomach via a nasogastric tube (NGT). After half an hour if > 400 mL is left in the stomach, the diagnosis of GOO is made.[31]
Needle-guided biopsy
Needle guided biopsy is used to evaluate patients for metastasis, in order to detect the primary tumor on histology.
Treatment
Medical Therapy
- Medical therapy may be given to all patients prior to surgery in cases of gastric outlet obstruction. Medical therapy primarily involves supportive care in preparation of surgery with hydration, NG tube decompression, correction of electrolyte imbalances. [32]
- Endoscopic stent placement for advanced GI cancer causing GOO.[33]
- In patients with benign Gastric Outlet Obstruction due to peptic ulcer disease, medical therapy with proton pump inhibitors or histamine-2 (H2) blockers is given in patients to treat acute inflammation and edema.[9]
- For the treatment of strictures in patients with GOO due to advanced stage cancer, endoscopic pneumatic balloon dilatation and use of self-expandable metallic stents are preferred techniques.[34]
Surgery
Surgery is the primary modality of treatment for patients with GOO. It is required for more than 75 percent of patients, with scarring, fibrosis and tumors. The aims of surgery in case of GOO include relief of obstruction, patients with failure to respond to medical therapy or failure to improve even after 72 hours of therapy, and correction of PUD symptoms.
Guidelines for surgery
Surgery should be considered only in patients who are able to tolerate the surgical procedure. Major resections of the tumor must be done in the absence of metastatic disease. In the case of metastatic disease, extent of surgery needs to be determined.
Types of surgical procedures
The types of surgical procedures performed in cases of GOO are as follows:[35][36][37]
- Vagotomy and antrectomy, gastrojejunostomy (vagotomy and antrectomy with Billroth II reconstruction), balloon dilatation, pylorotomy, pyloroplasty, robotic-assisted pyloroplasty, vagotomy and pyloroplasty, truncal vagotomy and gastrojejunostomy and laparoscopic surgery (laparoscopic truncal vagotomy, laparoscopic gastrojejunostomy, laparoscopic pyloromyotomy, laparoscopic gastrojejunostomy). The advantages of laparoscopy include fast GI transit recovery time, fewer blood transfusions, low mortality and brief hospital stay.
- Endoscopic surgery (Endoscopic gastroenteric anastomosis) is preferred in cases of malignant obstruction. The advantages include high success rate, brief hospital stay and low mortality.[38][39][40]
Contraindications to surgery
Contraindications to surgery include severe malnutrition and advanced unresectable cancer.
Complications of surgery
Complications arising after surgery include perforation due to stenting, stent reocclusion, stent migration, stomach dilation, gastric wall edema, anastomotic leak and postgastrectomy syndromes.[41][42]
References
- ↑ Bradley EL, Clements JL (1981). "Idiopathic duodenal obstruction: an unappreciated complication of pancreatitis". Ann. Surg. 193 (5): 638–48. PMC 1345138. PMID 7235767.
- ↑ Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK (1992). "Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history". Am. J. Gastroenterol. 87 (3): 337–41. PMID 1539568.
- ↑ Poley JW, Steyerberg EW, Kuipers EJ, Dees J, Hartmans R, Tilanus HW, Siersema PD (2004). "Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy". Gastrointest. Endosc. 60 (3): 372–7. PMID 15332026.
- ↑ Ciftci AO, Senocak ME, Büyükpamukçu N, Hiçsönmez A (1999). "Gastric outlet obstruction due to corrosive ingestion: incidence and outcome". Pediatr. Surg. Int. 15 (2): 88–91. doi:10.1007/s003830050523. PMID 10079337.
- ↑ Kreel L, Ellis H (1965). "Pyloric stenosis in adults: A clinical and radiological study of 100 consecutive patients". Gut. 6 (3): 253–61. PMC 1552275. PMID 18668780.
- ↑ Gheorghe L, Băncilă I, Gheorghe C, Herlea V, Vasilescu C, Aposteanu G (2002). "Antro-duodenal tuberculosis causing gastric outlet obstruction--a rare presentation of a protean disease". Rom J Gastroenterol. 11 (2): 149–52. PMID 12145672.
- ↑ 7.0 7.1 Urayama S, Kozarek R, Ball T, Brandabur J, Traverso L, Ryan J, Wechter D (1995). "Presentation and treatment of annular pancreas in an adult population". Am. J. Gastroenterol. 90 (6): 995–9. PMID 7771437.
- ↑ Johnson CD (1995). "Gastric outlet obstruction malignant until proved otherwise". Am. J. Gastroenterol. 90 (10): 1740. PMID 7572886.
- ↑ 9.0 9.1 9.2 Shone DN, Nikoomanesh P, Smith-Meek MM, Bender JS (1995). "Malignancy is the most common cause of gastric outlet obstruction in the era of H2 blockers". Am. J. Gastroenterol. 90 (10): 1769–70. PMID 7572891.
- ↑ Johnson CD, Ellis H (1990). "Gastric outlet obstruction now predicts malignancy". Br J Surg. 77 (9): 1023–4. PMID 2207566.
- ↑ Roy PK, Venzon DJ, Shojamanesh H, Abou-Saif A, Peghini P, Doppman JL, Gibril F, Jensen RT (2000). "Zollinger-Ellison syndrome. Clinical presentation in 261 patients". Medicine (Baltimore). 79 (6): 379–411. PMID 11144036.
- ↑ Sugimachi K, Inokuchi K, Kuwano H, Ooiwa T (1984). "Acute gastritis clinically classified in accordance with data from both upper GI series and endoscopy". Scand J Gastroenterol. 19 (1): 31–7. PMID 6710074.
- ↑ Sipponen P, Maaroos HI (2015). "Chronic gastritis". Scand J Gastroenterol. 50 (6): 657–67. doi:10.3109/00365521.2015.1019918. PMC 4673514. PMID 25901896.
- ↑ Sartor RB (2006). "Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis". Nat Clin Pract Gastroenterol Hepatol. 3 (7): 390–407. doi:10.1038/ncpgasthep0528. PMID 16819502.
- ↑ Sipponen P (1989). "Atrophic gastritis as a premalignant condition". Ann Med. 21 (4): 287–90. PMID 2789799.
- ↑ Badillo R, Francis D (2014). "Diagnosis and treatment of gastroesophageal reflux disease". World J Gastrointest Pharmacol Ther. 5 (3): 105–12. doi:10.4292/wjgpt.v5.i3.105. PMC 4133436. PMID 25133039.
- ↑ Ramakrishnan K, Salinas RC (2007). "Peptic ulcer disease". Am Fam Physician. 76 (7): 1005–12. PMID 17956071.
- ↑ Banasch M, Schmitz F (2007). "Diagnosis and treatment of gastrinoma in the era of proton pump inhibitors". Wien Klin Wochenschr. 119 (19–20): 573–8. doi:10.1007/s00508-007-0884-2. PMID 17985090.
- ↑ Dicken BJ, Bigam DL, Cass C, Mackey JR, Joy AA, Hamilton SM (2005). "Gastric adenocarcinoma: review and considerations for future directions". Ann Surg. 241 (1): 27–39. PMC 1356843. PMID 15621988.
- ↑ Ghimire P, Wu GY, Zhu L (2011). "Primary gastrointestinal lymphoma". World J Gastroenterol. 17 (6): 697–707. doi:10.3748/wjg.v17.i6.697. PMC 3042647. PMID 21390139.
- ↑ Lin KJ, García Rodríguez LA, Hernández-Díaz S (2011). "Systematic review of peptic ulcer disease incidence rates: do studies without validation provide reliable estimates?". Pharmacoepidemiol Drug Saf. 20 (7): 718–28. doi:10.1002/pds.2153. PMID 21626606.
- ↑ Sung JJ, Kuipers EJ, El-Serag HB (2009). "Systematic review: the global incidence and prevalence of peptic ulcer disease". Aliment. Pharmacol. Ther. 29 (9): 938–46. doi:10.1111/j.1365-2036.2009.03960.x. PMID 19220208.
- ↑ Green ST, Drury JK, McCallion J, Erwin L (1987). "Carcinoid tumour presenting as recurrent gastric outlet obstruction: a case of long-term survival". Scott Med J. 32 (2): 54–5. doi:10.1177/003693308703200212. PMID 3602991.
- ↑ Chowdhury A, Dhali GK, Banerjee PK (1996). "Etiology of gastric outlet obstruction". Am. J. Gastroenterol. 91 (8): 1679. PMID 8759707.
- ↑ Miner PB, Harri JE, McPhee MS (1982). "Intermittent gastric outlet obstruction from a pedunculated gastric polyp". Gastrointest. Endosc. 28 (3): 219–20. PMID 7129059.
- ↑ Cappell MS, Davis M (2006). "Characterization of Bouveret's syndrome: a comprehensive review of 128 cases". Am. J. Gastroenterol. 101 (9): 2139–46. doi:10.1111/j.1572-0241.2006.00645.x. PMID 16817848.
- ↑ Hangen D, Maltz GS, Anderson JE, Knauer CM (1989). "Marked hypergastrinemia in gastric outlet obstruction". J. Clin. Gastroenterol. 11 (4): 442–4. PMID 2760432.
- ↑ Chaudhuri TK, Greenwald AJ, Heading RC (1975). "Measurement of gastric emptying time--a comparative study between nonisotopic aspiration method and new radioisotopic technique". Am J Dig Dis. 20 (11): 1063–6. PMID 1199997.
- ↑ Lau JY, Chung SC, Sung JJ, Chan AC, Ng EK, Suen RC, Li AK (1996). "Through-the-scope balloon dilation for pyloric stenosis: long-term results". Gastrointest. Endosc. 43 (2 Pt 1): 98–101. PMID 8635729.
- ↑ Awan A, Johnston DE, Jamal MM (1998). "Gastric outlet obstruction with benign endoscopic biopsy should be further explored for malignancy". Gastrointest. Endosc. 48 (5): 497–500. PMID 9831838.
- ↑ Goldstein H, Boyle JD (1965). "The saline load test--a bedside evaluation of gastric retention". Gastroenterology. 49 (4): 375–80. PMID 5831782.
- ↑ Gouma DJ, van Geenen R, van Gulik T, de Wit LT, Obertop H (1999). "Surgical palliative treatment in bilio-pancreatic malignancy". Ann. Oncol. 10 Suppl 4: 269–72. PMID 10436838.
- ↑ Holt AP, Patel M, Ahmed MM (2004). "Palliation of patients with malignant gastroduodenal obstruction with self-expanding metallic stents: the treatment of choice?". Gastrointest. Endosc. 60 (6): 1010–7. PMID 15605026.
- ↑ Kozarek RA (1993). "Dilation therapy for gastric outlet obstruction. Are balloons a bust?". J. Clin. Gastroenterol. 17 (1): 2–4. PMID 8409292.
- ↑ Alam TA, Baines M, Parker MC (2003). "The management of gastric outlet obstruction secondary to inoperable cancer". Surg Endosc. 17 (2): 320–3. doi:10.1007/s00464-001-9197-0. PMID 12384765.
- ↑ Chopita N, Landoni N, Ross A, Villaverde A (2007). "Malignant gastroenteric obstruction: therapeutic options". Gastrointest. Endosc. Clin. N. Am. 17 (3): 533–44, vi–vii. doi:10.1016/j.giec.2007.05.007. PMID 17640581.
- ↑ Wong YT, Brams DM, Munson L, Sanders L, Heiss F, Chase M, Birkett DH (2002). "Gastric outlet obstruction secondary to pancreatic cancer: surgical vs endoscopic palliation". Surg Endosc. 16 (2): 310–2. doi:10.1007/s00464-001-9061-2. PMID 11967685.
- ↑ Kantsevoy SV, Jagannath SB, Niiyama H, Chung SS, Cotton PB, Gostout CJ, Hawes RH, Pasricha PJ, Magee CA, Vaughn CA, Barlow D, Shimonaka H, Kalloo AN (2005). "Endoscopic gastrojejunostomy with survival in a porcine model". Gastrointest. Endosc. 62 (2): 287–92. PMID 16046997.
- ↑ Chopita N, Vaillaverde A, Cope C, Bernedo A, Martinez H, Landoni N, Jmelnitzky A, Burgos H (2005). "Endoscopic gastroenteric anastomosis using magnets". Endoscopy. 37 (4): 313–7. doi:10.1055/s-2005-861358. PMID 15824939.
- ↑ No JH, Kim SW, Lim CH, Kim JS, Cho YK, Park JM, Lee IS, Choi MG, Choi KY (2013). "Long-term outcome of palliative therapy for gastric outlet obstruction caused by unresectable gastric cancer in patients with good performance status: endoscopic stenting versus surgery". Gastrointest. Endosc. 78 (1): 55–62. doi:10.1016/j.gie.2013.01.041. PMID 23522025.
- ↑ Jaffin BW, Kaye MD (1985). "The prognosis of gastric outlet obstruction". Ann. Surg. 201 (2): 176–9. PMC 1250637. PMID 3970597.
- ↑ Khullar SK, DiSario JA (1996). "Gastric outlet obstruction". Gastrointest. Endosc. Clin. N. Am. 6 (3): 585–603. PMID 8803569.